Neurofeedback Therapy for Enhancing Visual Attention: State-of-the-Art and Challenges

We have witnessed a rapid development of brain-computer interfaces (BCIs) linking the brain to external devices. BCIs can be utilized to treat neurological conditions and even to augment brain functions. BCIs offer a promising treatment for mental disorders, including disorders of attention. Here we review the current state of the art and challenges of attention-based BCIs, with a focus on visual attention. Attention-based BCIs utilize electroencephalograms (EEGs) or other recording techniques to generate neurofeedback, which patients use to improve their attention, a complex cognitive function. Although progress has been made in the studies of neural mechanisms of attention, extraction of attention-related neural signals needed for BCI operations is a difficult problem. To attain good BCI performance, it is important to select the features of neural activity that represent attentional signals. BCI decoding of attention-related activity may be hindered by the presence of different neural signals. Therefore, BCI accuracy can be improved by signal processing algorithms that dissociate signals of interest from irrelevant activities. Notwithstanding recent progress, optimal processing of attentional neural signals remains a fundamental challenge for the development of efficient therapies for disorders of attention

Electrolytic lesion of the nucleus raphe magnus reduced the antinociceptive effects of bilateral morphine microinjected into the nucleus cuneiformis in rats

Several lines of investigation show that the rostral ventromedial medulla is a critical relay for midbrain regions, including the nucleus cuneiformis (CnF), which control nociception at the spinal cord. There is some evidence that local stimulation or morphine administration into the CnF produces the effective analgesia through the nucleus raphe magnus (NRM). The present study tries to determine the effect of morphine-induced analgesia following microinjection into the CnF in the absence of NRM. Seven days after the cannulae implantation, morphine was microinjected bilaterally into the CnF at the doses of 0.25, 1, 2.5, 5, 7.5 and 10 μg/0.3 μl saline per side. The morphine-induced antinociceptive effect measured by tail-flick test at 30, 60, 90 and 120 min after microinjection. The results showed that bilateral microinjection of morphine into the CnF dose-dependently causes increase in tail-flick latency (TFL). The 50% effective dose of morphine was determined and microinjected into the CnF (2.5 μg/0.3 μl saline per side) in rats after NRM electrolytic lesion (1 mA, 30 s). Lesion of the NRM significantly decreased TFLs, 30 (P < 0.01) and 60 (P < 0.05) but not 90-120 min after morphine microinjection into the CnF, compared with sham-lesion group. We concluded that morphine induces the analgesic effects through the opioid receptors in the CnF. It is also appeared that morphine-induced antinociception decreases following the NRM lesion but it seems that there are some other descending pain modulatory pathways that activate in the absence of NRM

Analgesic effect of morphine microinjected into the nucleus raphe magnus after electrolytic lesion of nucleus cuneiformis in tail-flick and formalin tests in rat

Introduction: The antinociceptive effect of morphine is, in part, mediated through the activation of a descending pathway. One of the major components of this pathway is the nucleus raphe magnus (NRM). Our previous study demonstrated the involvement of NRM in the analgesic effect of morphine microinjected into the nucleus cuneiformis (NCF) in a descending manner. The aim of the current study was to investigate another aspect of the interaction between these two nuclei in both acute and chronic inflammatory pain models. Methods: In order to calculate 50% effective dose (ED50) of morphine, animals received bilateral morphine injections (1, 2.5, 5 and 10 μg/0.5 μl saline) into the NRM. The obtained ED50 of morphine was applied into the NRM with/without bilateral electrolytic lesion (500 μA, 30 sec) of the NCF. Tail-flick and formalin tests were applied as behavioral analgesic tests in this study. Results: Results interestingly showed that the intra-NRM morphine injection (ED50; 1 μg/0.5 μl saline) resulted in an increase in tail flick latencies (morphine-induced antinociception) at 30-min intervals, while bilateral electrolytic lesions in the NCF could notably decreased the morphine-induced antinociception during 30-90 min after the injection of morphine. Data also showed that bilateral morphine microinjected into the NRM, dose-dependently increases the antinociceptive responses during both early and late phases of formalin test. The antinociceptive effect of morphine microinjected into the NRM was significantly attenuated at the late phase but not early phase following the bilateral destruction of NCF in formalin test. Conclusion: It could be concluded that there is a reciprocal interaction between NRM and NCF during morphine - induced antinociception in both acute and chronic inflammatory pain models in rat